Durrheim et al., Safety of Travel in Kruger National Park...

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South Africa is a flourishing tourist destination andthe South African Tourism Board (SATOUR) recordeda steady growth in international visitors of about 11% perannum for the period from 1994–1999.1 The four mostpopular sites visited by tourists are Cape Town and envi-rons, the Garden Route,Oudtshoorn ostrich farms, andthe Kruger National Park. The Kruger National Park(KNP), which at over 1.949 million hectares, is thelargest wildlife or nature reserve in a single Africancountry, affords the visitor the opportunity to appreci-ate a magnificent variety of flora and fauna, in their nat-ural environment (Fig. 1). In 1998 almost one milliontourists visited the KNP.1

In recent years, the various infamous titles bestowedon South Africa, including the dubious dual distinctionof being referred to as the world’s “rape and high-jackingcapitals,” have reputedly slowed the projected 20% perannum tourism growth in South Africa (personal com-munication,Dale Pretorius,CEO,SATOUR,Jan.2000).Extensive press coverage of South African epidemics,including cholera, bovine tuberculosis, and malaria,

appear to have negatively influenced the volume oftourism to the KNP. Although it is not possible todirectly measure the impact by contacting all peopleconsidering a visit but deciding against it because ofperceived risk, the proportional monthly distribution ofvisitors is informative.When considering overnight vis-itor numbers, available from the Kruger National ParkCommercial Development and Tourism database forthe period April 1997 to March 2000 inclusive, it isnoteworthy that only 17.8% of visitors stayed in theKNP during the January to March quarter. This is thetime-period commonly perceived by the media to be ofhighest malaria risk. The impact of negative media per-ceptions of malaria risk is particularly apparent for Jan-uary 2000. Widespread media panic followeddeterioration of the malaria situation in KwaZulu-Natal.The lowest proportion (3.8%) of residential visitors of anymonth in the past 4 years occurred in January 2000,com-pared with an average of 6.6% for January during the pre-vious 3 years (Fig. 2). Media coverage of a choleraoutbreak during February 1998 in rural Mpumalanga wasalso accompanied by a decrease in residential visitors,decreasing to 4.6% for that month, compared with anaverage of 5.6% for the month of February from1997–2000.

The image of safety in African nature reserves has beentarnished by a number of criminal activities in recentyears.2 Travelers have encountered life-threatening situa-tions from armed bandits in East Africa. An increase inarmed conflicts, especially in northeastern and centralAfrica, has made military automatic and semi-automaticweapons easily available for use in robberies and attacks.Public concern is fueled by media reports and specific fea-tures of nature reserves ensure that actual or perceived unto-ward events in the reserve or surrounding environmentwill be newsworthy. Factors found to characterize news-worthiness include novelty, seriousness, potential for epi-demic spread, the bizarre nature of an event, humaninterest and drama, all elements that could be present.3

Although a central tenet of travel medicine is thatprevention should be based on epidemiological data,limited attempts have been made to formally catalogue

REVIEW ARTICLES

Safety of Travel in South Africa: The Kruger National ParkDavid N. Durrheim, Leo Braack, Douw Grobler, Helena Bryden, Rick Speare,and Peter A. Leggat

David N. Durrheim, MPH, FACTM: Consultant inCommunicable Disease Control, Mpumalanga Departmentof Health, South Africa; L.E.O. Braack, PhD: TransfrontierConservation Planning Coordinator, South African NationalParks; Douw Grobler, BVSc, MSc: Manager—Game Capture,Kruger National Park; Helena Bryden, BSc (Hons):Biotechnician, Scientific Services, Kruger National Park; RickSpeare, PhD, FACTM, FAFPHM: Associate Professor, Schoolof Public Health and Tropical Medicine, James CookUniversity, Australia; Peter A. Leggat, FAFPHM, FACTM:Associate Professor, School of Public Health and TropicalMedicine, James Cook University, Australia.

The authors had no financial or other conflicts of interest todisclose.

Reprint requests: Dr. David N. Durrheim, Consultant inCommunicable Disease Control, Mpumalanga Departmentof Health and Adjunct Associate Professor, School of PublicHealth and Tropical Medicine, James Cook University,Townsville, Australia.

J Travel Med 2001; 8:176–191.

Durrhe im et a l . , Safe ty o f Trave l in Kruger Nat iona l Park 177

Figure 1 The Kruger National Park in relation to Africa and southern Africa.

and quantify the hazards encountered by tourists visit-ing African nature reserves, and the KNP in particular.4

Currently, recommendations of travel medicine advisors,and risk-modifying measures adopted by travelers, arelargely based on anecdote, personal opinion, and relatednonscientific approaches. An additional strategy used toestimate risk to travelers, particularly for infectious dis-eases, is extrapolation from local population data.5 Thisapproach has major weaknesses, as routine demographicand disease notification data in African countries are noto-riously inaccurate.6 In addition,most tourists enjoy con-siderably safer environments than rural populations thatbear the brunt of these health-related events.Tourists typ-ically consume food and water of higher microbiologi-cal quality,are exposed to fewer mosquito bites,have betteraccess to medicines and medical assistance, and may havea better understanding of disease and its prevention,than most local residents in developing countries. Thususing country level malaria, schistosomiasis, rabies, foodand waterborne diseases, tuberculosis, and arboviral dis-ease prevalences, to estimate risk for travelers to theKNP may not be appropriate.

The object of the present review is to cataloguepotentially important health-related conditions that existin the KNP,attempt to provide a realistic appraisal of riskwithin the limits of available data, and briefly describemeasures taken by the KNP administration to modify spe-

cific risks. A broad variety of information sources wereexploited to obtain these data including a comprehen-sive review of published and unpublished scientificresearch conducted in the KNP,commercial press records,postal and in-flight surveys,police records of criminal andtraffic offenses, local general practice records, and inter-views with key informants. Various routine databases,including the food-handler screening program, abattoirrecords, water monitoring records, and notificationrecords of statutory notifiable medical conditions werealso used. This methodology has the limitations inher-ent to studies utilizing retrospective data sources notspecifically designed for use in research. Although thismeans that exact risks could not be quantified, it was alsoadvantageous, removing potential Hawthorne effectsthat might have existed if data collection had been setup prospectively.7

Vector-Borne Diseases

MalariaMalaria accounts for 9% of all disease in Africa, and

over one million people,mainly small children,die frommalaria annually.8 Recently there has been an increasein malaria prevalence in Africa, and four factors areincriminated: resistance of Plasmodium falciparum parasitesto chloroquine and sulfadoxine-pyrimethamine; resistance

1 7 8 Journal of Trave l Medic ine , Volume 8, Number 4

Figure 2 Proportional monthly overnight visitors, Kruger National Park, April 1996–March 2000.

of Anopheline mosquitoes to insecticides;climate changes;and large-scale migration.9,10 South Africa has also beenaffected, and the past three decades have seen a greaterthan 100-fold increase in the number of malaria casesnotified to the National Department of Health, from 364cases in 1971 to 51,433 cases in 1999.11 This is despitea residual intradomicillary spraying program that hasseen the distribution of malaria in South Africa reducedby 80% and limited to the northeastern areas borderingMozambique, Swaziland, and Zimbabwe.12 Novelapproaches,guided by operational research, including theseminal introduction of rapid malaria diagnostic tests atprogram level, exploiting mosquito vector behavior forcost-effective community control measures, and employ-ing high-resolution geographical information systems(GIS) for planning and evaluating control, have seennotable improvements in malaria control and manage-ment in Mpumalanga Province,which adjoins the south-ern KNP.13–15

South African health authorities use seasonal malariaincidence at district level to guide malaria chemopro-phylaxis recommendations for tourists.16 Although avail-able GIS capabilities allow a finer resolution, and timelydefinition of risk in rural communities resident withinthe malaria area, it is naïve to equate the risk in rural vil-lages with that of tourists in wildlife reserves, like the KNP.Factors contributing to this disparate risk include lengthof stay in the malarious area, location of dwelling in rela-tion to vector breeding sites,disproportionate cost of mostcommercially available personal protection measures tolocal residents, and type of accommodation used. Usingrates of malaria in villagers adjacent to the KNP may over-estimate the risk of malaria to travelers, and lead tounnecessary use of antimalarial prophylaxis, with asso-ciated drug-related adverse events.17

To more accurately quantify malaria risk to visitorsto the KNP, a postal survey was conducted during 1996in the large cohort of visitors that stayed in the KNP dur-ing the month of April.18 This was an epidemic year, andApril was chosen because this is a higher risk malariamonth,with a relative increase of 89.6% over the monthlyaverage of reported malaria cases in South Africa.19 Theattack rate of 4.5 cases of P. falciparum malaria per 10,000visitors during April, is not only much lower than thatin the highest risk rural communities in MpumalangaProvince, South Africa, 20 per 1,000 per annum, but itcompares very favorably with the malaria risk defined invisitors to other popular African destinations e.g., 30 per10,000 visitors per month for travelers to Kenya.15,20 Indeciding whether malaria prophylaxis should be advo-cated, it is essential to establish whether the risk ofmalaria outweighs the risk of serious prophylaxis asso-ciated side-effects.Although no association was demon-strated between malaria risk and use of chemoprophylaxis,

since the risk of serious neuropsychiatric side-effectswith, for example, mefloquine is 1 in 10,000, thereappears to be merit in promoting use of effective anti-malarial medications at least during the summer rainfallmonths.21 This period extends from September to Mayin the KNP.

It would be ideal to continuously monitor travel-ers to generate relevant risk estimates, but unfortunatelythis is not feasible, as annual large-scale postal surveys areresource-intensive.However, it may be possible to approx-imate malaria risk trends in visitors, from the incidenceof malaria in KNP employees. This proxy risk trend isprobably valid because employees are also not believedto enjoy any immunity due to the seasonal nature ofmalaria in South Africa. Employees’ risk represents anupper risk limit, as they perform duties outdoors dur-ing the peak nocturnal vector-biting period, and few, ifany, employees utilize malaria chemoprophylaxis. Staffmembers are continually cautioned to maintain a high-index of suspicion of any febrile symptoms, and toimmediately seek medical care and definitive diagnosis,that is immediately available within the KNP. Thesecases are notified by general practitioners located in theKNP.The rates amongst employees during the past 4 yearswere 12.6% (1996), 4.4% (1997), 5.8% (1998) and 8.6%(1999) per annum. The lack of an increase of casesamongst KNP employees, since the time of the travelersurvey,provides reassurance that the risk of malaria to vis-itors is unlikely to have escalated, if their incidence is areliable proxy measure of risk to travelers.

However, research into KNP visitors’knowledge andbehavior indicates that there remain opportunities for fur-ther reducing personal malaria risk.Although the major-ity of visitors surveyed during the peak malaria seasonused either chloroquine and proguanil in combination(35.6%),or mefloquine (18.4%),a sizeable proportion usedregimens not recommended in this chloroquine-resistantarea, including chloroquine alone (15.7%).22 Only 30%of travelers using prophylaxis reported being fully com-pliant,using antimalarial drugs both regularly as prescribedand for 4 weeks after leaving the malaria area.23 Althoughthis finding is similar to that of a study in Kenyan trav-elers, it is a source of concern, as severe malaria is moreoften the result of premature cessation of drug, than ofusing the wrong drug.20,24

KNP visitors’ use of personal measures to avoidmosquito bites and their knowledge of malaria are alsoinadequate. Despite the safety record of topical N,N-diethyl-m-toluamide (DEET) containing insect-repellent,use and evidence of the value of adequate clothing cover,insecticide and/or coils, air conditioning and/or bednets,and repellents for reducing malaria risk, these measuresare underutilized by KNP visitors.25,26 A postal surveyfound that 13% of visitors used no personal protection


against mosquito bites during the highest risk season,andonly 17% used four or more effective measures.27 A dis-concerting finding of a survey amongst in-flight passengersreturning from Skukuza Airport in the KNP, was thatmore than a third of travelers did not recognize fever orflu-like illness, as an important symptom of malaria.28

A remote warm water spring with a unique breed-ing colony of Anopheles arabiensis Patton mosquitoes,the dominant malaria vector in South Africa,has provena valuable site for seminal research on the behavior of thesevectors for improved cost-effective malaria prevention.29,30

Research has shown that the peak biting activity of An.arabiensis is during the predawn period, and that 81% ofbites occur on the ankles or feet.31 Wearing closed shoes,or raising feet off the ground, dramatically reduces vec-tor contact, as does application of small doses of DEETcontaining insect repellent to the feet, without redistri-bution of bites to more proximal body parts.32 The valueof various locally available commercial and plant-derivedrepellents for reducing bites is also currently beingassessed.

In addition to conducting essential research, theKNP routinely embarks on a number of actions toreduce malaria.All residential units are sprayed twice peryear with a residual synthetic pyrethroid insecticide(deltamethrin), and windows and doors are fitted withmosquito-proof gauze.Larvaciding with Bacillus thuringien-sis is performed in residential camps, and to a diameterof 300 meters outside. This is extended to 800 metersduring high incidence years, when a helicopter is used.The KNP advocates the use of antimalarial chemopro-phylaxis during the malaria risk months and personal pro-tection measures against mosquitoes throughout theyear. Malaria information brochures are available atentrance gates, reception offices, shops, and on the Inter-net.33,34 Mosquito repellents, coils and vaporizing matsare available in all camp shops for purchase by visitors.Two doctors, equipped with malaria diagnostic tests,and effective therapy, are available at the largest camp,Skukuza.

ArbovirusesChikungunya, an alphavirus, and dengue and yellow

fever,both flaviviruses, are mosquito-borne diseases mostdramatically associated with a hemorrhagic fever picture.Rift Valley fever, a phlebovirus, also relies on a mosquitovector for survival and transmission, and infrequentlycauses human disease in South Africa.35

Chikungunya is a mosquito-borne virus of Africaand Asia that causes febrile illness with a maculopapu-lar rash and protracted arthralgia of a variable numberof joints. Wild primates serve as reservoir hosts of thevirus.36 Although anthropophilic populations of Aedesaegypti, the most efficient vector mosquito,reach high den-

sities along the KwaZulu-Natal and Eastern Cape coastduring summer, such populations are rare in inlandSouth Africa.37 This absence of anthropophilic A.aegyptimay explain why the three previously recorded humanoutbreaks of Chikungunya virus, in Mpumalanga andNorthern Province, that border the KNP, remained focalin rural savannah areas. These outbreaks (1956,1975/1976, and 1977) involved epizootic transmissionbetween baboons and vervet monkeys, and the sylvaticmosquito, Aedes furcifer, following heavy rains and resul-tant high densities of these treehole breeding mosqui-toes.38–43 A. aegypti was not involved in any of theseoutbreaks.

Dengue fever is not endemic in South Africa andprevious occurrences resulted from importation of casesinto the Durban area of KwaZulu-Natal from the Indiansubcontinent.44 Although Natal coastal A. aegypti havebeen shown experimentally to be competent vectors ofDengue virus, South African A. furcifer, which is foundin the KNP, is a poor vector of Dengue 1 and 2 viruses.45

In Africa,yellow fever is a tropical disease of West andCentral Africa that does not occur in South Africa.Its intro-duction into South Africa is considered highly unlikelyas this would require a person who had not received pro-tective vaccine to be infected from a sylvatic source in ruralSouth America or Africa and then rapidly travel to SouthAfrica in the summer months to infect man-biting A.aegypti. As already emphasized, anthropophilic A. aegyptiis restricted to the eastern coast of the country,and there-fore there is no risk of yellow fever in the KNP.46

Rift Valley fever (RVF) was first recognized as a majorepizootic in South Africa, during 1950/1951 with theloss of approximately 100,000 sheep and cattle, andapproximately 500,000 abortions in sheep.47 Concurrentdisease in humans, characterized by a febrile illness withtransient loss of visual acuity, was recognized.48,49 In thesecond documented South African outbreak, during1975, seven human deaths resulted and were associatedwith either acute hemorrhagic fever or encephalitis.50–52

Epizootics occur periodically following heavy rainsthat flood natural depressions.This allows hatching of theprimary vector and reservoir (Aedes spp) mosquitoesthat have become infected by trans-ovarial transmissionof RVF virus.53–57 Additional RVF outbreaks haveoccurred in South Africa, one on the inland plateauthat affected sheep farming areas following heavy rains(1974–1976) and a small outbreak in coastal northernKwaZulu-Natal in 1981.

People have rarely been affected during these RVFepizootics, and human involvement is usually restrictedto veterinary workers, or those involved in the livestockindustry, where exposure to viremic tissues of freshlyslaughtered or aborted infectious animals, is a risk fac-tor. This assertion is supported by experience from the


latest outbreak in South Africa, and the only one toaffect the KNP. During late January 1999, abortionsoccurred in pregnant buffaloes, with deaths in a fewother species, including giraffe.Three veterinary officialsinvolved in conducting autopsies on these animals alsodeveloped a mild febrile disease after becoming infectedwith the virus. However, there is believed to be no riskto visitors to national parks (R Swanepoel, personalcommunication,Feb.1999) in South Africa, as the mos-quito vector is zoophilic, and seldom ventures indoors,and visitors rarely have direct contact with wild animals.

Ecologically there is a very slight likelihood of out-breaks of Chikungunya and Rift Valley fever in the KNP,but no risk exists for either dengue or yellow fever. Yel-low fever vaccination is therefore not indicated if SouthAfrica is the only African destination. If an outbreak ofeither Chikungunya or RVF occurs in the KNP,then mea-sures to prevent mosquito bites would be a sensible pre-caution. Visitors who remain within their vehicles, asprescribed by the KNP, are believed to be at almost norisk,as they would not be exposed to preferred vector habi-tats, or to fresh carcasses, or aborted wildlife fetuses.

Tick-Borne DiseasesHard ticks (Ixodidae) are vectors of tick bite fever

(Rickettsia conorii and Rickettsia africae), Q-fever (Coxiellaburneti) and Congo-Crimean hemorrhagic fever in south-ern Africa. Large numbers of birds and wild mammalshave been examined for infestation with ixodid ticks inthe KNP. Every warthog (Phacochoerus aethiopicus),Burchell’s zebra (Equus burchelli), impala (Aepyceros melam-pus), and kudu (Tragelaphus strepsiceros) examined wasfound to be infested with Amblyomma hebraeum, partic-ularly the immature tick stages.58 Larger host mammalspecies carried a greater burden of adult ticks, in partic-ular eland, buffalo, giraffe, and rhinoceros.

Other ixodid tick species, including Boophilus decol-oratus,have also been found to commonly infest large wildruminant mammals in KNP, and Haemaphysalis spp andRhipicephalus spp commonly infest wild carnivores,whereas Hyalomma truncatum predominantly infests scrubhares (Lepus saxatilis).59–63 Investigations into the sea-sonal abundance of ticks on wild ruminants found adistinct increase during drought years.64–66 Collection offree-living ticks, by means of drag-sampling with flan-nel strips, resulted in the collection of 14 tick species,withAmblyomma hebraeum and Boophilus decoloratus, predom-inating.67

African tick bite fever. African tick bite fever, is a febriledisease characterized by classical eschars, with or with-out skin rash,and occasionally complicated by severe mul-tisystem disease, particularly if diagnosis and effectivetherapy is delayed.68,69 The two forms seen are Mediter-ranean spotted fever which is caused by Rickettsia conorii

and transmitted by Rhipicephalus sp, and classical Africantick bite fever, caused by Rickettsia africae and transmit-ted by Amblyomma hebraeum. A growing number ofreports of tick bite fever being diagnosed in travelersreturning from visits to South African nature reserves haveappeared.70–74 However, the true incidence rate is notknown because most travelers have returned home beforethe completion of the incubation period. Incidenceamongst staff members can be used as a proxy measureof risk to travelers.Medical records indicate that this variesfrom 1 to 4 cases per month, with a peak in the sum-mer months. This value is probably an extreme upperlimit, because of increased opportunities for exposure ofstaff to ticks. However, it may indicate that tick bitefever is a more important disease entity for travelersthan presently recognized. People walking in high grassshould wear clothes that cover their bodies, particularlytheir legs, and apply effective tick repellents on exposedskin, or impregnate their clothes with permethrin.

Vervet monkeys may also be infected with R. conoriiin the KNP.36 Monkeys and other small mammals dooccasionally venture into camps and carry ticks with them.However, the risk of these ticks transferring to humanswithin a residential camp is believed to be remote.Crimean-Congo hemorrhagic fever. Crimean-Congo hem-orrhagic fever (CCHF), caused by infection with anairovirus, infrequently causes human disease in SouthAfrica.35 This virus occurs in eastern Europe, Asia, andAfrica in a distribution that corresponds with the mainvectors of the virus: ticks of the genus Hyalomma. Theseticks are known as pied-leg ticks in South Africa withtheir alternating rufous-brown and white leg banding.Ticks are infected when their immature stages feed onviremic small mammals, like hares. Adult ticks, infectedas larvae or nymphs, subsequently feed on large ani-mals, like cattle,horses, zebra, and antelope, and transmitinfection.There is no evidence of domestic livestock orwildlife becoming sick from CCHF infection, but theyare briefly viremic.75

During this period their tissues are infectious to peo-ple,particularly during butchering or postmortem.For-tunately, the virus does not survive well in tissues afterdeath and so does not constitute a hazard in meatprocessed according to health regulations.76

People become infected either by contact withfreshly slaughtered livestock (cattle, sheep, or ostriches),contact with infected fluids from patients, from tickbites,or from squashing ticks.35,77,78 Despite documentedwide distribution of antibody in the sera of cattle and wildvertebrates, there have been no human CCHF casesrecorded as a result of contact with infectious tissues fromfreshly slaughtered wildlife in South Africa.77,79

The majority of ticks implicated are H. truncatum,although specimens of H. marginatum rufipes and H. m.


turanicum have also been incriminated.80,81 These ticks onlyhave one life cycle per annum,and adults are more activein summer and immature stages peak in autumn and win-ter.82 Fortunately the three species of Hyalomma ticks thatoccur in South Africa rarely feed on humans, althoughticks may bite people if there is prolonged contact, e.g.,when lying on a tick on the ground.76,83

There is no documented occupational risk, or riskto visitors, in the KNP. Walking trail participants maychoose to plan their trips for seasons when ticks areleast active. Accommodation on walking trails does notinclude sleeping on the ground,but hikers should be cau-tioned to treat clothing with insecticides, e.g., syntheticpyrethroids, especially socks and pants, and apply repel-lent to exposed skin.

Other Zoonotic Diseases

AnthraxAnthrax is a potentially lethal disease in humans,

which may follow inhalation, or ingestion, of the sporesof the causative bacterium,Bacillus anthracis.84 Most oftenhowever, human disease follows direct contact withanthrax-infected animals, or anthrax-contaminated ani-mal products, occasionally with dramatic results as cor-roborated by an outbreak of more than 10,000 cases ofcutaneous anthrax in Zimbabwe between 1979 and1985.85 Vegetative bacteria have a poor survival outsidea mammal host,of less than 24 hours.86 This contrasts withthe phenomenally hardy spores that can survive fordecades in an inhospitable environment.87 The spores ger-minate in an environment rich in glucose, amino acids,and nucleosides, such as mammalian tissues, and the veg-etative bacilli form spores if there is a deficiency of thesenutrients, most notably when infected body fluids areexposed to air.

Evidence from genotype grouping indicates thatanthrax is an indigenous disease in the KNP, and thatsouthern Africa may have been the geographical originof B. anthracis.88 Anthrax is an important wildlife diseaseand has caused serious losses in wild animal populationsin the KNP. During epidemic outbreaks in 1959, 1960,1970,1990,1991,1993, and 1999,more than 5,000 wildanimals succumbed.89 The disease occurs endemically inPafuri, in the far north of the KNP, and periodically inepidemic form in other areas.90

A variety of animal species have been affected,with kudu antelope (Tragelaphus strepsiceros) being thefocus of many epidemics.The density of susceptible kuduappears to be an important factor for maintaining thedisease in the KNP.The contribution of blowflies as dis-seminators of the disease amongst kudus has been estab-lished.91 Carnivores, particularly lions (Panthera leo), havealso been affected largely through feeding on the car-

casses of buffalo (Syncerus caffer) at water holes andtroughs.92 Lions open carcasses providing the opportu-nity for sporulation of the anthrax bacilli, and dissem-ination of spores.93 Vultures also play an effectivedisseminator role due to their scavenging habits and wideflight ranges.94

The reassuring finding of rapidly declining numbersof anthrax spores with distance downwind from heav-ily infected anthrax carcass sites,makes the likelihood ofinfection by inhalation while in transit near a carcass sitehighly improbable.95

Hides from carcasses infected with B. anthracis areregarded as being permanently infected and may con-taminate articles with which they come into contact.Evenfinal products made after the tanning or curing of rawhides are not necessarily free from spores and thus noproducts from anthrax-infected wildlife are harvested orsold in the KNP.96 Interestingly, the infectivity of anthraxspores for humans is normally regarded as low.97 Dur-ing the anthrax epidemics in KNP wildlife, large teamsof workmen were used to track down, sometimes cut up,and burn anthrax contaminated carcasses. They weredefinitely exposed, but only one contracted cutaneousanthrax after suffering a puncture wound from a bonefragment.90 Further,no mishap took place during the fieldnecropsies of more than 50 anthrax carcasses in the KNP(De Vos, in preparation).There is no risk to tourists unlessthey ignore KNP rules and leave their vehicle and han-dle an infected carcass.

Bovine TuberculosisTuberculosis (TB) caused by Mycobacterium bovis is

clinically indistinguishable from TB caused by Mycobac-terium tuberculosis, and has been confirmed from a num-ber of African countries.98 Although the consumptionof milk contaminated by M.bovis is regarded as the prin-cipal mode of transmission between animals and humans,agricultural workers may acquire the disease by inhalingcoughed particles from infected cattle.99,100

Bovine tuberculosis due to M. bovis, was diagnosedfor the first time, in an emaciated African buffalo (Synceruscaffer), in the southern KNP in July 1990.101 Since thattime bovine tuberculosis has been demonstrated com-monly in African buffalo in the southern KNP, and insome buffalo herds the prevalence is as high as 70%.102

The distribution and characteristics of pulmonarylesions in certain buffalo suggest that the initial route ofinfection is aerogenous and the cavernous state of thesepulmonary lesions indicates that such animals were prob-ably highly infective at the time of death.102 The survivaltime of M.bovis in the natural habitat of infected free rang-ing wildlife has been investigated, and it could only beisolated for a maximum period of 6 weeks from infectedtissue specimens, and for 4 weeks from feces.103


Spillover into other species, including cheetah (Aci-nonyx jubatus), lions (Panthera leo), and chacma baboons(Papio ursinus),has been documented,and this raised a con-cern about the potential of transmission of M. bovis tohumans.104

This led to an investigation amongst KNP employ-ees considered at high risk of infection, including work-ers involved in slaughtering tuberculous buffalo.105

Screening for active disease was performed by bacteri-ological investigation of sputum specimens using stan-dard laboratory methodology, and study participants alsounderwent comparative intradermal skin testing to deter-mine their level of infection. For comparative purposes,testing was also done in low risk groups, including work-ers involved in handling carcasses after butchering, andin a group of workers who were not considered to beat risk, including administrative workers.M.bovis was notisolated from any of the 206 employees tested, neitherdid differential skin testing show any degree of M. bovisinfection risk, even among high risk occupations. Rea-sons for this low risk may include the performance ofhigh-risk procedures, slaughtering and post mortems, inthe open, with an abundance of sunlight and fresh air,and thus dilution of infectious aerosols.106

As bovine tuberculosis was not found to be an occu-pational zoonosis in the Park, nor was aerosol transmis-sion demonstrated as a mechanism for human infectionin this study, there is not believed to be any meaningfulrisk to tourists.105

RabiesRabies virus, lyssavirus 1, is generally transmitted by

the bite of infected animals, and causes fatal encephali-tis in humans and other warmblooded vertebrates. Thedisease is widely distributed in the world, and was diag-nosed for the first time in Africa in 1893, in the EasternCape Province.107 South Africa is endemic for rabies,beinghyperendemic in yellow mongoose (Cynictis penicillata)on the central plateau of the country.108 The maintenancehost in the dry western areas is the bat-eared fox (Oto-cyon megalotis), and the black-backed jackal (Canis mesome-las) fills this niche in the northern parts of the countrybordering Zimbabwe.109 More than 90% of the 10–20cases of human rabies that are recorded annually, occurin KwaZulu-Natal,where dog rabies has been intractablesince re-introduction into this province in 1976.

Rabies has not been diagnosed in wildlife in theKNP despite active attempts at detection, and there istherefore no risk to visitors.110

PlagueIn the recent past there has been a resurgence of epi-

demic plague globally, and this is particularly an Africanproblem,where nearly 65% of the 3,000 annually reported

cases occur.111 Rodents, in particular veld rats (Aethomyschrysophilus) in the KNP, are infested with Xenopsyllabrasiliensis, the flea that maintains plague circulation inrodent populations in Africa, and that is capable of trans-mitting the infection to humans.112

Serological surveys for antibodies against the plaguebacillus,Yersinia pestis, are useful tools for detecting plaguefoci,and monitoring the efficacy of control measures.113,114

Recently revived serological plague surveillance in dogsand rodents,with concurrent flea indices determinationin Mpumalanga Province, includes a rural district, Shon-gwe, bordering the KNP, and no evidence of plagueinfection has been found.115 There have been no reportedhuman plague cases in South Africa since 1982, whenplague was diagnosed in the coastal regions of the East-ern Cape.116 The most eastern extent of plague detectedin Mpumalanga is more than 200 km west of the KNPboundary.117

Sleeping SicknessTsetse fly (Glossina morsitans morsitans) occurred his-

torically in the KNP until the large-scale Rinderpestoutbreak during 1896 decimated its animal hosts. TheMozambican civil war caused suspension of collaborativefly control in southern Africa and currently no informationexists on the southward movement of flies in Mozambique.Tsetse flies recolonize former habitats at a rate of 5–10km per year.118 Therefore, an early warning surveillancesystem was established in the KNP in 1982 to monitorthe incursion of tsetse flies into the Limpopo/Levuvhudrainage system. Twelve modified Harris traps wereerected at strategic locations along the river courses to trapflies. In addition, thick blood smears are now taken in thefar north of the KNP in buffaloes and other mammals,and examined for the presence of trypanosomes on anannual basis during the rainy summer period (Februaryand March). Although numerous blood-sucking flies ofthe genera Haematopota,Tabanus, and Stomoxys have beencollected,no Glossina spp have been collected,and no pos-itive serology detected. There is therefore no risk ofNagana, or sleeping sickness in the KNP.

African Horse SicknessAfrican horse sickness (AHS) is common in zebra

foals from the KNP and six serotypes have beendescribed.119 However,disease, subclinical and clinical, asa result of infection with AHS has only been describedonce in humans.Four laboratory workers from the samevaccine-packing facility developed, at different timesover an 8-year period, an illness characterized byencephalitis (in 3 workers) and uveochorioretinitis (in 4)after aerosol exposure, as a result of accidental breakageof freeze-dried vaccine bottles.120,121 There is thereforeno risk to KNP visitors.


Encephalomyocarditis VirusEncephalomyocarditis virus infection has been asso-

ciated with cardiac failure and fatality in African elephants(Loxodonta africana) since 1987 in the KNP. In a singleoutbreak that began in December 1993, peaked in Jan-uary 1994, and terminated by November 1994, 64 ele-phants died.122 Studies conducted on rodents in theKNP demonstrated a remarkable temporal correlationbetween the outbreak in elephants and a rodent popu-lation explosion.There was a concurrent increase in theprevalence of encephalomyocarditis virus antibodies inrodents.

All staff members who had exposure to infectedrodents or elephants were carefully screened for serologicalactivity and symptoms.Only 2 staff members who wereinvolved in sampling over 900 mice and performingpost mortems on 20 elephants, had serological evidenceof infection, and only 1 of these suffered a mild headachefor a few days. There thus appears to be no risk to visi-tors to the KNP; indeed encephalomyocarditis’ status asa zoonotic disease remains to be confirmed.

Foot-and-Mouth DiseaseFoot-and-mouth disease (FMD) is the most eco-

nomically important viral disease of livestock.The KNPis a foot-and-mouth endemic area, and a routine sur-veillance program of cloven-hoofed animals is operatedto monitor FMD activity.123 South African Territory(SAT) types of FMD virus are maintained in buffalo(Syncerus caffer) in the KNP, and there are regular out-breaks of FMD in impala (Aepyceros melampus), proba-bly as a result of transmission from carrier buffalo.124,125

In impalas FMD virus may circulate for a considerableperiod of time.

Measures to prevent the escape of the virus intodomestic animal populations adjacent to the KNP havebeen implemented, in particular the erection of a dou-ble fenced off corridor.Experimental work has shown thatthe risk of transmission from KNP buffalo carrying SATtypes 1, 2, and 3 viruses separated by a fence from FMDsusceptible cattle, but sharing common drinking troughsand hay racks for a 15-month period, was low.126

Reports of human infection with FMD are rare, andusually result from skin inoculation, or drinking conta-minated milk.127 No human cases have ever been diag-nosed in the KNP.128

Food and Waterborne Diseases

The meat from many wildlife species is pleasantlypalatable and popular amongst local people andtourists.129–131 Fortunately, very few pathogens are suf-ficiently robust to survive the significant changes in tem-perature, pH, moisture content, and osmolality which

occur post mortem,or which are associated with preser-vation processes such as pickling, smoking, or dry-ing.132 To ensure meat safety, a number of practices areobserved in the KNP. Carcasses are eviscerated in thefield immediately after slaughter, work is restricted tothe later afternoons to avoid hot conditions, and car-casses are transported with their skin to avoid conta-mination and bacterial decomposition. In the field,workers wear overalls, industrial gloves, and gum boots.The general hygiene at the meat processing plant ismaintained in terms of all conditions stipulated in theAbattoir Hygiene Act (Act 121 of 1992). This includesthorough cleaning and sterilization of equipment, reg-ular maintenance of all cooling facilities, and becauseall workers involved in meat processing, including theslaughter team, are considered food-handlers, they aremedically examined and tested for diseases transmissi-ble by food handling.

The Division of Veterinary Services based in theKNP conducts formal meat inspections in terms of theAbattoir Hygiene Act.This includes inspection for par-asitic cysts, tubercles, and abscesses.133 Bacterial counts areroutinely performed on biltong, and all canned meat isstored in brine with a pH tested below 5.5.Random sam-pling and culturing is done.

Since 1983, the KNP has employed a full time tech-nician to perform testing of samples, collected fromfood-handlers during medical examinations, that areconducted twice annually. A person who tests positiveis notified and relieved from duty immediately.They arereferred to the KNP doctor for treatment and onlyallowed to return to their duty after they have labora-tory proof of successful treatment. In addition supervi-sors are obliged to refer any employee with a chroniccough, gastrointestinal tract symptoms, or a skin condi-tion, to the doctor for treatment.For the 10-year period,1990-1999 inclusive,of 7,117 tests performed,1 was pos-itive for Shigella sp, 3 were positive for Salmonella typhi,and 28 were positive with Salmonella sp and referred forcurative therapy. During the same period, 9 food-han-dlers were diagnosed with pulmonary tuberculosis (TB).

Only pasteurized milk is sold or used in restau-rants. All fresh produce (bread, meat, fruit, and vegeta-bles) sold inside the Park is prepacked.Camp restaurantsare subjected to random quality-assurance inspections.Each region of the Park has its own Health and SafetyCommittee that carries out regular inspections in allcamps. Monthly meetings are held to address findings.The Training Section conducts training programsthroughout the year, including courses on occupationalhealth and safety, and occupational hygiene (includingpersonal hygiene). Each supervisor is expected to sendat least 5% of his/her staff on these courses each year.TheDepartments of Health of Mpumalanga and Northern


Provinces also perform inspections of facilities from timeto time.

BrucellosisBrucella abortus has been isolated from free-living wild

African buffalo (Syncerus caffer), and hippo, in theKNP.134,135 The serological prevalence is about 20% inhippo and 17% in buffalo.136 No known cases have everbeen detected amongst staff members, including veteri-nary personnel.The latter are at greatest risk when per-forming rectal examinations for pregnancy diagnosis.

TrichinosisIn Africa trichinosis is essentially a disease of wild

carnivores.137 The absence of trichinosis in true herbi-vores has been confirmed in the KNP,which is of impor-tance given the increasing utilization of game meat asfood. People would thus have to ingest undercookedinfested meat from a carnivore to become infected. Nohuman cases have ever been diagnosed in the KNP.

EchinococcosisEchinococcosis has been diagnosed in the follow-

ing wild species in the KNP: lion (Panthera leo), spottedhyena (Crocuta crocuta),Cape hunting dog (Lycaon pictus),Burchell’s zebra (Equus burchelli antiquorum), buffalo(Syncerus caffer),hippopotamus (Hippopotamus amphibius),and impala (Aepyceros melampus).138 Infestation rates in her-bivores vary from 60% in zebra to less than 1% in impala.Screening of high-risk staff has not yielded any positiveserology for echinococcosis (Braack LEO, unpublisheddata). There is no risk to tourists.

SalmonellaSalmonella sp infection is common in many wildlife

species, in particular crocodiles (Crocodylidae spp).139 Test-ing for Salmonella sp infection is routinely conducted oncarcasses in the abattoir. In addition,crocodiles should notbe handled, and crocodile meat is not processed, or soldin the KNP.

Water QualityStream water is provided for domestic use in res-

idential camps and bushcamps on walking trails aresupplied by bore holes. All raw water is purified usinga process including addition of flocculents, sedimenta-tion, filtration, and disinfection with chlorine. Freeresidual chlorine levels are determined on a daily basisand full biochemical and microbiological monitoringis conducted on a weekly basis.Review of registers indi-cates excellent water quality post-treatment. In addi-tion, investigation of river water and hippopotami(Hippopotamus amphibious) in the KNP revealed a lackof heavy metal pollution.140 For the more wary trav-

eler, all shops, restaurants, and cafeterias, sell sealed bot-tled water.

Other Infectious Conditions

Review of available general practice records, aninterview with the senior general practitioner at Skukuza,and perusal of statutory notifications, indicate that therehave been no cases of cholera, meningococcal menin-gitis or other formidable contagious conditions,diagnosedin the KNP for the 10-year period, 1990–1999 inclu-sive.

TuberculosisThe 1% prevalence of active disease with Mycobacterium

tuberculosis, detected among staff members during the M.bovis survey, and routinely detected in food-handlersthrough the screening program, is typical of communitytrends in South Africa.105,141 The active detection programamongst food-handlers,and referral of all employees withchronic cough of longer than 3 weeks for medical atten-tion by supervisors and a nursing sister located at Skukuza,limits the risk to visitors.

BilharziaThe eastern half of South Africa is endemic for

Schistosoma haematobium, and within this area there arehyperendemic foci of Schistosoma mansoni infection.142,143

The intermediate snail hosts exist in KNP waterways thatoriginate in areas where infected children may contam-inate them.Occasionally,Mozambican refugees could alsoplay this role.144

In southern Africa, Schistosoma mattheei infects cat-tle,horses, sheep,zebra,baboon,and antelope.145 AlthoughS. mattheei can infect people, it is almost always togetherwith S. haematobuim, or S. mansoni.146 The female of S.mattheei may in fact need a adult male S.haematobuim, orS. mansoni to transport it to its egg laying site.147

Thus, all streams and other natural water bodieswithin the KNP should be treated as infested with schis-tosomes. Park authorities do not permit swimming, orfishing, in streams, rivers,or dams, and have provided safechlorinated swimming pools in specific restcamps.Touristsshould thus be at no risk of contracting bilharzia in theKNP, as crocodiles and hippos provide a persuasive dis-incentive to swimming.

Trauma

The burden of trauma as a cause of death in the agegroup 15–60 years is greater in subSaharan Africa thanin any other region of the world.148 South Africa has aparticularly poor record,with the national per capita vio-lence mortality rate being one of the highest in the


world,and six times greater than the US.149 Of equal con-cern is the high traffic death rate per unit of distance trav-eled, that is only surpassed by Kenya, Morocco, andKorea.150 As traumatic events are not random occurrences,they are usually preventable.151

Wild Mammal AttacksAttacks by wild mammals can be exceptionally

newsworthy, whether these involve workers on naturereserves,or tourists.A review of commercial press recordsof all reported deaths and injuries to workers on wildlifereserves in South Africa from January 1988 to Decem-ber 1997 inclusive, found that 6 workers had been killedand 14 injured in encounters with wild mammals.152

Twelve of these incidents, including 4 deaths (2 soldiers,a gatekeeper,and a trail guide),occurred in the KNP.Nineincidents involved leopards or lions and elephants; buf-falo and giraffe accounted for the remaining episodes.Allattacks, with the exception of those involving leopards,occurred on foot, outside the safety of fenced camps.

Little was known about tourist risk of injury and deathby wild mammals in South Africa’s nature reserves beforea recent 10-year retrospective review of commercial pressrecords was conducted.153 Seven tourists were killed by wildmammals in South Africa between January 1988 andDecember 1997 inclusive.None of these tourist fatalitiesoccurred in the KNP,despite this being the most frequentlyvisited nature reserve. Three of the 4 deaths ascribed tolions in this study resulted from tourists carelessly approach-ing prides on foot, in lion reserves, and a private reserveprovided inadequate protection to a guest who was mauled.Tourist ignorance of animal behavior, and flagrant disre-gard of rules,contributed to the 2 fatalities involving hip-popotami.A bull elephant with severe discomfort from adental problem was responsible for the final death.

During the same period there were 14 nonfatalattacks on tourists, including 5 by hippo, 3 by buffalo, 2by rhino, and 1 each by a lion, leopard, zebra, and musthelephant. Four of these attacks occurred in the KNP,with hippo, leopard, rhino, and elephant, each involvedin a single attack. Only the incident with the elephant,occurred while the visitor was in their motor vehicle.Thisoccurred when an amorous bull elephant,disturbed whilesoliciting an elephant cow’s attention, charged a visitor’svehicle, and dragged it several meters after capsizing it.The injuries that resulted could have been prevented ifthe visitor had interpreted the warning display that pre-cedes an elephant’s charge, including the tell-tale temporalsecretion characterizing musth, ground-kicking, sway-ing motion, extended ears, and raised trunk with trum-peting.The action of a visitor who left his motor vehicle,in direct defiance of KNP rules, to examine a supposedlyinjured hippopotamus,was rewarded with a trampling,andminor injuries.The clawing of a camper at the Berg-en-

Dal camping site in the southern KNP by a leopard,wasunusual, as leopards seldom attack humans unless they aresick,or injured,or in defense.Leopards however,have thepropensity to enter open windows, or open tent flaps, asin this case.Windows should therefore be closed and tentssecurely zipped.

The attack by four black rhino on a walking trail par-ticipant on the Napi walking trail is informative, as itemphasizes the aggression of these large herbivores, par-ticularly if surprised. It is therefore essential that walk-ing trail participants not move too quietly and insist ona well-qualified trail guide. The KNP only uses guideswho are highly trained to standards set by the FieldGuides Association of South Africa with SKS/DA (spe-cial skills and dangerous animal training). This is clearlyworthwhile as demonstrated by the attack on a walkingtrail group by two angry lionesses. The experiencedranger leading the expedition shot one lioness and theother fled, without human injury.

An important reason that may explain the low num-ber of these incidents are the measures taken by KNPauthorities to prevent direct contact between wild mam-mals and tourists.This is largely through providing secureresidential camps that are completely fenced, includingelectrification. Visitors are not permitted to leave theirvehicles except at designated secure areas, and makethemselves liable for prosecution if they contravene.TheKNP employs topgraded guides to lead hiking trails, andthere are rangers available at camps to enlighten visitorson important animal behavior that may herald aggres-sion.

Motor Vehicle AccidentsLow speed limits of 50 km/h are enforced on good

quality tarred roads, and the limit on dust roads is 40km/h.A strict curfew is maintained,with no private vehi-cles allowed outside camps during the hours of darknessand heavy penalties are imposed to ensure the safety oftravelers and wildlife.154 These precautions are of particularrelevance when considering hippos that exhibit nocturnalgrazing behavior.

During the past ten years (1990–1999 inclusive)there have been no traffic-related human deaths in theKNP. There have been a total of 1,014 minor accidentswithin the KNP, adjoining private nature reserves, andon feeder public roads, but with only 45 injuries. Manyof these accidents either occurred in parking areas, orresulted from sudden stops without the driver behindnoticing.During this period,only 15 drivers were chargedwith reckless driving.

Natural DisastersIn the past quarter of a century there have been 6

fires that have affected residential camps. One in Lower


Sabie was caused by an electrical fault, and the other 5were the result of lightning, including the razing of thePretoriuskop Restaurant.There were no human injuriesor deaths. The only wind damage in the past quarter ofa century in the KNP has been to windmills.

Twice in the past 25 years there have been floodsin the KNP associated with tropical cyclones, in 1976,and 2000. Fortunately, these only resulted in damage toinfrastructure, particularly roads and bridges, and therewere no human casualties, or injuries.

Snake-BiteThere are a number of venomous snakes in the

KNP, including boomslang (Dispholidus typus typus),Mozambique spitting cobra (Naya mossambica),Egyptiancobra (Naya haje annulifera), and black mamba (Den-droaspis polylepis). In general, they avoid human contactthrough ferocious displays, flight,or feigning death.155 Aparticular problem however, is the puff adder (Bitis ari-etans arietans), that relies on immobility and cryptic cam-ouflage to avoid detection, basks in the sun on forestfootpaths, and thus may pose a risk to walking trail par-ticipants. However, well-trained trail guides lead groupsof people in single-file, and they carefully search forsnakes. It is remarkable that only 1 trail-participant hasbeen bitten by a snake in the past 20 years, and ironicallythis was by an African rock python, which is a nonven-omous snake.

Conclusions

Studies of risk perception assist us in understandingpublic response to health-related events in African naturereserves, and the attendant,often disproportionate, alarmthat these occurrences,or even theoretical threats, invoke.Research has shown that particular categories of healthevents more often provoke alarm in members of the pub-lic. These include exposures that are unusual, result indeaths that are vivid, occur in environments that areforeign to the individual, and where the effects of expo-sure may be delayed.156

This review of all available relevant data-sourcesindicates that tourists visiting the KNP are extremelyunlikely to experience any serious health-related con-dition as a direct result of their visit. To minimize thisrisk further a number of sensible precautions should betaken:

• Careful use of personal protection measures againstvector mosquitoes of malaria, from dusk to dawn,throughout the year.

• Correct use of effective malaria chemoprophylaxis,at least during the higher risk malaria months,Octo-ber to May.

• Topical application of effective tick repellents, andtreatment of socks and trousers with a syntheticpyrethroid to prevent tick bites,particularly if walk-ing on a trail.

• Remaining in a secure motor vehicle, or ade-quately fenced precincts while in the vicinity oflarge mammals.153

• Rigidly observing nature reserve instructions.• Never approaching animals that appear ill, mal-

nourished, displaying aggressive behavior traits, orfemales with young.154

• Checking the credentials of game rangers beforeembarking on a walking trail.152

• Ensuring adequate travel insurance, includingaeromedical evacuation contingency plans.157

From this review, it is clear that KNP managementhave taken all reasonable measures to reduce the incidenceof preventable injury,or illness, in visitors.Travelers havethe prime responsibility to educate themselves aboutrisks at their destination, how to assess these risks, andto take measures to minimize their personal exposure torisky situations.

References

1. South African Tourism Board.A survey of South Africa’s inter-national tourism market. Pretoria: South African TourismBoard, 1999.

2. Leggat PA, Klein M. Personal safety advice for travelersabroad. J Travel Med 2001; 8:46–51.

3. de Semir V. What is newsworthy? Lancet 1996; 347:1163–1166.

4. Steffen R. Travel medicine—prevention based on epidemi-ological data.Trans R Soc Trop Med Hyg 1991;85:156–162.

5. Waner S. Health risks of travelers in South Africa. J TravelMed 1999; 6:199–203.

6. Durrheim DN, Harris BN, Speare R, Billinghurst K. Infec-tion control nurses—sentinels for outbreak surveillance.BullWorld Health Organ 2001; 79:22–27.

7. Koontz H, Weihrich H. Management. 9th Ed. Singapore:McGraw Hill, 1989:35–36.

8. Kondrachine AV,Trigg P.Malaria:hope for the future.WorldHealth 1995; 2:26–27.

9. Nchinda TC.Malaria: a reemerging disease in Africa.EmergInfect Dis 1998; 4:398–403.

10. Marsh K. Malaria disaster in Africa. Lancet 1998; 352:924.11. Durrheim DN, Ogunbanjo GA, Blumberg L. Managing re-

emergent malaria in South Africa. S Afr Fam Pract 1999;21:19–24.

12. Sharp BL, le Sueur D.Malaria in South Africa—the past, thepresent and selected implications for the future. S Afr MedJ 1996; 86:83–89.

13. Durrheim DN, la Grange JJP, Govere J, Mngomezulu NM.Accuracy of a rapid immunochromatographic card test forPlasmodium falciparum in a malaria control programme inSouth Africa. Trans R Soc Trop Med Hyg 1998; 92:32–33.



14. Speare R,Govere J,Durrheim DN.Malaria control in SouthAfrica: symposium in the wilderness. J Travel Med 1999;6:149–150.

15. Booman M,Durrheim DN,La Grange JJP,et al.Using a geo-graphical information system to plan a malaria control pro-gramme in South Africa. Bull World Health Organ 2000;78:1438–1444.

16. Department of Health. Guidelines for the prophylaxis ofmalaria. Pretoria: Department of Health, 1996.

17. Dollow S.Risk-benefit ratios must be taken into account.BMJ1996; 313:1553.

18. Durrheim DN, Braack LEO, Waner S, Gammon S. Risk ofmalaria in visitors to the Kruger National Park,South Africa.J Travel Med 1998; 5:173–177.

19. Uyirwoth GC. Malaria notifications in South Africa. Epi-demiol Comments 1995; 22:165–174.

20. Lobel HO, Phillips-Howard PA, Brandling-Bennett AD, etal. Malaria incidence and prevention among European andNorth American travellers to Kenya. Bull World HealthOrgan 1990; 88:209–215.

21. Lonergan G.Antimalarials for visitors to Kruger National Park?J Travel Med 1999; 6:210.

22. Durrheim DN, Gammon S, Waner S, Braack LEO. Anti-malarial prophylaxis—use and adverse events in visitors to theKruger National Park. S Afr Med J 1999; 89:170–175.

23. World Health Organization.Malaria prophylaxis for travellers.Wkly Epidemiol Rec 1993; 68:377–383.

24. Behrens RH. Chloroquine and proguanil prophylaxis intravellers to Kenya. Lancet 1992; 339:63.

25. Fradin MS.Mosquitoes and mosquito repellents: a clinician’sguide. Ann Intern Med 1998:128:931–940.

26. Schoepke A,Steffen R,Gratz N.Effectiveness of personal pro-tection measures against mosquito bites for malaria prophy-laxis in travellers. J Travel Med 1998; 5:188–192.

27. Durrheim DN, Leggat PA. Prophylaxis against malaria.Preventing mosquito bites is also effective. BMJ 1999;318:1139.

28. Waner S,Durrheim D,Braack LEO,Gammon S.Malaria pro-tection measures used by in-flight travelers to South Africangame parks. J Travel Med 1999; 6:254–257.

29. Coetzee M, Braack LEO. Anopheles arabiensis in the KrugerNational Park. Proceedings of the 8th Entomological Con-gress of the Entomological Society of Southern Africa,Bloemfontein, 1–4 July 1991. Johannesburg: EntomologicalSociety of Southern Africa, 1991:19.

30. Coetzee M, Hunt RH, Braack LEO, Davidson D. Distribu-tion of mosquitoes belonging to the Anopheles gambiae com-plex, including malaria vectors, south of the latitude 15°S. SAfr J Sci 1993; 89:227–231.

31. Braack LEO,Coetzee M,Hunt RH,et al.Biting pattern andhost-seeking behavior of Anopheles arabiensis (Diptera: Culi-cidae) in northeastern South Africa. J Med Entomol 1994;31:333–339.

32. Govere J, Braack LEO, Durrheim DN, et al. Effects on thebiting pattern of Anopheles arabiensis mosquitoes in the KrugerNational Park, South Africa after treating human ankles andfeet with a mosquito repellent. In press.

33. National Parks Board, Pretor ia, South Afr ica.http://www.parks-sa.co.za/malariainfopage.

34. National Parks Board, Pretor ia, South Afr ica.http://www.parks-sa.co.za/knp/scientificservices/FAQS.

35. Swanepoel R.Viral haemorrhagic fevers in South Africa:his-tory and national strategy. S Afr J Sci 1987; 83:80–88.

36. Kaschula VR,Van Dellen AF, de Vos V. Some infectious dis-eases of wild vervet monkeys (Cercopithecus aethiops pygerythrus)in South Africa. J S Afr Vet Assoc 1978; 49:223–227.

37. Kemp A, Jupp PG.Potential for dengue in South Africa:mos-quito ecology with particular reference to A. aegypti. J AmMosq Control Assoc 1991; 7:574–583.

38. McIntosh BM, Jupp PG, Dos Santos I. Rural epidemic ofchikungunya in South Africa with involvement of Aedes(Diceromyia) furcifer (Edwards) and baboons.S Afr J Sci 1977;73:267–269.

39. Fourie ED, Morrison JGL. Rheumatoid arthritic syndromeafter chikungunya fever. S Afr Med J 1979; 56:130–132.

40. Morrison JGL. Chikungunya fever. Int J Dermatol 1979;18:628–629.

41. Jupp PG. Aedes (Diceromyia) furcifer (Edwards) and Aedes(Diceromyia) cordellieri Huang in southern Africa: distribu-tion and morphological differentiation. J Am Mosq ControlAssoc 1998; 14:273–276.

42. Jupp PG, McIntosh BM. Aedes furcifer and other mosquitoesas vectors of chikungunya virus at Mica,northeastern Trans-vaal, South Africa. J Am Mosq Control Assoc 1990;6:415–420.

43. Jupp PG, McIntosh BM, Dos Santos I, DeMoor P. Labora-tory vector studies on six mosquito and one tick species withchikungunya virus. Trans R Soc Trop Med Hyg 1981;75:15–19.

44. Blackburn NK, Rawat R. Dengue fever imported fromIndia. S Afr Med J 1987; 71:386–387.

45. Jupp PG,Kemp A.The potential for dengue in South Africa:vector competence tests with dengue 1 and 2 viruses and 6mosquito species. Trans R Soc Trop Med Hyg 1993;87:639–643.

46. Jupp PG,Kemp A.What is the potential for future outbreaksof chikungunya,dengue and yellow fever in southern Africa.S Afr Med J 1996; 86:35–37.

47. Alexander RA. Rift Valley fever in the Union. J S Afr VetMed Assoc 1951; 22:105–109.

48. Gear JHS.Rift Valley fever in South Africa.S Afr Med J 1951;25:620.

49. Freed I. Rift Valley fever in man complicated by retinalchanges and loss of vision. S Afr Med J 1951; 25:930–932.

50. Van Velden DJJ, Meyer JD, Olivier J, et al. Rift Valley feveraffecting humans in South Africa. S Afr Med J 1977;51:867–871.

51. Gear JHS.Haemorrhagic fevers of Africa.An account of tworecent outbreaks. J S Afr Vet Assoc 1977; 48:5–8.

52. McIntosh BM, Russel D, dos Santos I, Gear JHS. Rift Valleyfever in humans in South Africa. S Afr Med J 1980;58:803–806.

53. World Health Organization. An outbreak of Rift ValleyFever, Eastern Africa, 1997–1998. Wkly Epidemiol Rec1998; 73:105–109.

54. McIntosh BM, Jupp PG, Anderson D, Dickinson DB. RiftValley fever. 2. Attempts to transmit virus with seven speciesof mosquito. J S Afr Vet Med Assoc 1973; 44:57–60.


55. Jupp PG,Cornel AJ.Vector competence tests with Rift Val-ley fever virus and five South African species of mosquito. JAm Mosq Control Assoc 1988; 4:4–8.

56. McIntosh BM, Jupp PG. Epidemiological aspects of RiftValley fever in South Africa with reference to vectors. Con-trib Epidemiol Biostat 1981; 3:92–99.

57. Linthicum KJ,Davies FG,Kairo A,Bailey CL.Rift Valley fever(family Bunyaviridae, genus Phlebovirus). Isolations fromDiptera collected during the inter-epizootic period in Kenya.J Hyg (Cambridge) 1985; 95:197–209.

58. Horak IG, MacIvor KM, Petney TN, De Vos V. Some avianand mammalian hosts of Amblyomma hebraeum and Amblyommamarmoreum (Acari: Ixodidae).Onderstepoort J Vet Res 1987;54:397–403.

59. Horak IG, De Vos V, De Klerk BD. Parasite of domestic andwild animals in South Africa. XVII. Arthropod parasites ofBurchell’s zebra, Equus burchelli, in the eastern TransvaalLowveld. Onderstepoort J Vet Res 1984; 51:145–154.

60. Horak IG, Boomker J, Spickett AM, De Vos V. Parasites ofdomestic and wild animals in South Africa. XXX. Ectopar-asites of kudus in the eastern Transvaal Lowveld and the east-ern Cape Province. Onderstepoort J Vet Res 1992;59:259–273.

61. Horak IG,Potgieter FT,Walker JB,et al.The ixodid tick bur-dens of various large ruminant species in South Africannature reserves.Onderstepoort J Vet Res 1983;50:221–228.

62. Horak IG, Guillarmod AJ, Moolman LC, de Vos V. Parasitesof domestic and wild animals in South Africa. XXII. Ixodidticks on domestic dogs and on wild carnivores. Onder-stepoort J Vet Res 1987; 54:573–580.

63. Horak IG, Spickett AM, Braack LEO, et al. Parasites ofdomestic and wild animals in South Africa. XXXIII. Ixodidticks on scrub hares in the north-eastern regions of north-ern and eastern Transvaal and of KwaZulu-Natal. Onder-stepoort J Vet Res 1995; 62:123–131.

64. Spickett AM, Horak IG, Heyne H, Braack LEO. The effectof severe drought on the abundance of ticks on vegetationand on scrub hares in the Kruger National Park.Koedoe 1995;38:59–64.

65. Horak IG, De Vos V, Braack LEO. Arthropod burdens ofimpalas in the Skukuza region during two droughts in theKruger National Park. Koedoe 1995; 38:65–71.

66. Horak IG. The relationship between ticks, hosts and theenvironment in the Kruger National Park, South Africa.Proceedings of the Second International Conference onTick-borne Pathogens at the Host-vector Interface:A GlobalPerspective. Kruger National Park August 28–September 1,1995.Pretoria:Onderstepoort Veterinary Institute 2:413–426.

67. Spickett AM, Horak IG, Braack LEO, van Ark H. Drag-sampling of free-living ixodid ticks in the Kruger NationalPark. Onderstepoort J Vet Res 1991; 58:27–32.

68. Loubser MD,Davies VA,Meyers KE,Christianson AL.Severeillness caused by Rickettsia conorii. Ann Trop Paediatr 1993;13:277–280.

69. Walker DH, Gear JH. Correlation of the distribution ofRickettsia conorii, microscopic lesions, and clinical features inSouth African tick bite fever. Am J Trop Med Hyg 1985;34:361–371.

70. Puente S, Lago M, Subirats M, et al. Spotted fever attribut-able to Rickettsia conorii: ten cases imported from subSaharanAfrica. J Travel Med 1995; 2:204–205.

71. Raeber P,Winteller S,Paget J.Fever in the returned traveller:remember rickettsial disease. Lancet 1994; 344:331.

72. Jensenius M,Hasle G,Henriksen AZ, et al.African tick-bitefever imported into Norway: presentation of 8 cases. ScandJ Infect Dis 1999; 31:131–133.

73. Fournier PE,Beytout J,Raoult D.Tick-transmitted infectionsin Transvaal: consider Rickettsia africae. Emerg Infect Dis1999; 5:178–181.

74. Brouqui P,Harle JR,Delmont J, et al.African tick-bite fever.An imported spotless rickettsiosis. Arch Intern Med 1997;157:119–124.

75. Burt FJ, Swanepoel R, Braack LEO. Enzyme-linkedimmunosorbent assays for the detection of antibody toCrimean-Congo haemorrhagic fever virus in the sera oflivestock and wild vertebrates. Epidemiol Inf 1993;111:547–557.

76. Hoogstraal H. The epidemiology of tick-borne Crimean-Congo haemorrhagic fever in Asia, Europe, and Africa: areview article. J Med Entomol 1979; 15:307–417.

77. Swanepoel R, Shepherd AJ, Leman PA, et al. Epidemiologicand clinical features of Crimean-Congo hemorrhagic feverin southern Africa. Am J Trop Med Hyg 1987; 36:120–132.

78. Joubert JR,King JB,Rossouw DJ,Cooper R.A nosocomialoutbreak of Crimean-Congo haemorrhagic fever at Tyger-berg Hospital. S Afr Med J 1985; 68:722–728.

79. Shepherd AJ, Swanepoel R, Shepherd SP, et al. Antibody toCrimean Congo hemorrhagic fever virus in wild mammalsfrom southern Africa.Am J Trop Med Hyg 1987;36:133–142.

80. Cummings GS.Host preference in African ticks (Acari: Ixo-dida): a qualitative data set. Bull Entomol Res 1998;88:379–406.

81. Swanepoel R, Struthers JK, Shepherd AJ, et al. Crimean-Congo hemorrhagic fever in South Africa. Am J Trop MedHyg 1983; 32:1407–1415.

82. Horak IG. Parasites of domestic and wild animals in SouthAfrica.XV.The seasonal prevalence of ectoparasites on impalaand cattle in the Northern Transvaal.Onderstepoort J Vet Res1982; 49:85–93.

83. Theiler G. The Ixodoidea parasites of vertebrates in Africasouth of the Sahara.Report to the Director of Veterinary Sci-ences, Pretoria: Onderstepoort Veterinary Institute 1962,Project 9958.

84. Inglesby TV, Henderson DA, Bartlett JG, et al. Anthrax as abiological weapon. Medical and public health management.JAMA 1999; 281:1735–1745.

85. Myenye KS, Siziya S, Peterson D. Factors associated withhuman anthrax outbreak in the Chikupo and Ngandu vil-lages of Murewa district in Mashonaland East Province,Zim-babwe. Cent Afr J Med 1996; 42:312–315.

86. Titball RW, Turnbull PC, Hutson RA. The monitoring anddetection of Bacillus anthracis. J Appl Bacteriol 1991;70:95–185.

87. Williams RP.Bacillus anthracis and other spore forming bacilli.In: Braude AI, Davis LE, Fiere J, eds. Infectious disease andmedical microbiology. Philadelphia: WB Saunders,1986:270–278.


88. Smith KL, De Vos V, Bryden HB, et al. Meso-scale ecologyof anthrax in southern Africa: a pilot study of diversity andclustering. J Appl Microbiol 1999; 87:204–207.

89. De Vos V,Bryden HB.Anthrax in the Kruger National Park:temporal and spatial patterns of disease occurrence.SalisburyMed Bull 1996; 87:26–31.

90. Pienaar U de V.Epidemiology of anthrax in wild animals andthe control of anthrax epizootics in the Kruger National Park,South Africa. Fed Proc 1967; 26:1496–1502.

91. Braack LEO, De Vos V. Feeding habits and flight range ofblow-flies (Chrysomyia spp) in relation to anthrax transmis-sion in the Kruger National Park, South Africa. Onder-stepoort J Vet Res 1990; 57:141–142.

92. De Vos V. Anthrax. In: Coetzer JAW, Thomson GR, TustinRC, eds. Infectious diseases of livestock with special refer-ence to southern Africa. Cape Town: Oxford UniversityPress, 1994:1262–1289.

93. McConnell EE, Tustin RC, de Vos V. Anthrax in an Africanbuffalo (Syncerus caffer) in the Kruger National Park. J S AfrVet Assoc 1972; 43:181–187.

94. Lindeque PM, Turnbull PC. Ecology and epidemiology ofanthrax in the Etosha National Park,Namibia.OnderstepoortJ Vet Res 1994; 61:71–83.

95. Turnbull PC, Lindeque PM, Le Roux J, et al. Airbornemovement of anthrax spores from carcass sites in the EtoshaNational Park,Namibia. J Appl Microbiol 1998;84:667–676.

96. Henning MW. Anthrax. Animal diseases in South Africa.Johannesburg: CNA, 1956.

97. Watson A, Keir D. Information on which to base assess-ments of risk from environments contaminated with anthraxspores. Epidemiol Infect 1994; 113:479–490.

98. Cosivi O, Grange JM, Daborn CJ, et al. Zoonotic Tubercu-losis due to Mycobacterium bovis in developing countries.Emerg Infect Dis 1998; 4:59–70.

99. Collins CH, Grange JM. A review. The bovine tuberclebacillus. J Appl Bacteriol 1983; 55:13–29.

100. Moda G, Daborn CJ, Grange JM, Cosivi O. The zoonoticimportance of Mycobacterium bovis. Tuber Lung Dis 1996;77:103–108.

101. Bengis RG,Kriek NP,Keet DF, et al.An outbreak of bovinetuberculosis in a free-living African buffalo (Syncerus caffer Spar-rman) population in the Kruger National Park: a preliminaryreport. Onderstepoort J Vet Res 1996; 63:15–18.

102. Keet DF,Kriek NP,Huchzermeyer H,Bengis RG.Advancedtuberculosis in an African buffalo (Syncerus caffer Sparrman).J S Afr Vet Assoc 1994; 65:79–83.

103. Tanner M,Michel AL. Investigation of the viability of M.bovisunder different environmental conditions in the KrugerNational Park. Onderstepoort J Vet Res 1999; 66:185–190.

104. Keet DF, Kriek NP, Penrith ML, et al. Tuberculosis in buf-faloes (Syncerus caffer) in the Kruger National Park: spread ofthe disease to other species. Onderstepoort J Vet Res 1996;63:239–244.

105. Weyer K, Fourie PB, Durrheim D, et al. Mycobacterium bovisas a zoonosis in the Kruger National Park, South Africa. IntJ Tuberc Lung Dis 1999; 3:1113–1119.

106. Weyer K, Fourie PB, Durrheim DN, et al. Mycobacteriumbovis infection in workers in the Kruger National Park. Pro-ceedings of the ARC-Onderstepoort OIE International

Congress with WHO-Cosponsorship on Anthrax, Brucel-losis,CBPP,Clostridial and Mycobacterial Diseases,Berg-en-Dal,Kruger National Park,South Africa, 9–15 August 1998.Onderstepoort: Onderstepoort Veter inary Institute,1998:383–387.

107. Hutcheon D.Reports of the Colonial Veterinary Surgeon andAssistant Veterinary Surgeons for the year 1893.Cape of GoodHope: Department of Agriculture, 1894.

108. Swanepoel R, Barnard BJH, Meredith CD, et al. Rabies insouthern Africa.Onderstepoort J Vet Res 1993;60:325–346.

109. Barnard BJH. The role played by wildlife in the epizootiol-ogy of rabies in South Africa and South West Africa.Onder-stepoort J Vet Res 1979; 46:155–163.

110. Meredith CD. Wildlife rabies: past and present in SouthAfrica. S Afr J Sci 1982; 78:411–415.

111. Gubler DJ.Resurgent vector-borne diseases as a global healthproblem. Emerg Infect Dis 1998; 4:442–450.

112. Braack LEO, Horak IG, Jordaan LC, et al. The comparativehost status of red veld rats (Aethomys chrysophilus) and bushveldgerbils (Tatera leucogaster) for epifaunal arthropods in thesouthern Kruger National Park,South Africa.OnderstepoortJ Vet Res 1996; 63:149–158.

113. Shepherd AJ, Leman PA. Plague in South African rodents1972–1981.Trans R Soc Trop Med Hyg 1983;77:208–211.

114. Gordon HG, Isaacson M, Taylor P. Plague antibody in largeAfrican mammals. Infect Immun 1979; 26:767–769.

115. Govere J, Durrheim DN, Booman A. Plague surveillance inSouth Africa. S Afr Med J 1999; 89:570.

116. Shepherd AJ, Hummitzsch DE, Leman PA, Hartwig EK.Studies on plague in the Eastern Cape Province of SouthAfrica. Trans R Soc Trop Med Hyg 1983; 77:800–808.

117. Hallett AF. A serological survey of the small mammals forplague in southern Africa. S Afr Med J 1970; 44:829–834.

118. Laid M. Tsetse: the future biological methods in integratedcontrol. Ottawa: IDRC, 1977.

119. Lord CC, Woolhouse ME, Barnard BJ. Transmission anddistribution of virus serotypes: African horse sickness inzebra. Epidemiol Infect 1997; 118:43–50.

120. Swanepoel R,Erasmus BJ,Williams R,Taylor MB.Encephali-tis and chorioretinitis associated with neurotropic African hors-esickness virus infection in laboratory workers. Part III.Virological and serological investigations. S Afr Med J 1992;81:458–461.

121. van der Meyden CH,Erasmus BJ,Swanepoel R,Prozesky OW.Encephalitis and chorioretinitis associated with neurotropicAfrican horsesickness virus infection in laboratory workers.Part I. Clinical and neurological observations. S Afr Med J1992; 81:451–454.

122. Grobler DG, Raath JP, Braack LEO, et al. An outbreak ofencephalomyocarditis-virus infection in free-ranging Africanelephants in the Kruger National Park. Onderstepoort J VetRes 1995; 62:97–108.

123. Mpumalanga Directorate of Veterinary Services. Annualreport. Nelspruit: Directorate of Veterinary Services, 1999.

124. Thomson GR,Vosloo W,Esterhuysen JJ,Bengis RG.Main-tenance of foot and mouth disease viruses in buffalo (Synceruscaffer Sparrman, 1779) in southern Africa. Rev Sci Tech1992; 11:1097–1107.


125. Keet DF, Hunter P, Bengis RG, et al. The 1992 foot-and-mouth disease epizootic in the Kruger National Park. J S AfrVet Assoc 1996; 67:83–87.

126. Bengis RG, Thomson GR, Hedger RS, et al. Foot-and-mouth disease and the African buffalo (Syncerus caffer). 1.Car-riers as a source of infection for cattle. Onderstepoort J VetRes 1986; 53:69–73.

127. Morgan-Capner P, Bryden AS. Foot-and-mouth disease,vesicular stomatitis,Newcastle disease, and swine vesicular dis-ease. In:Palmer SR,Soulsby EJL,Simpson DIH,eds.Zoonoses.Oxford: Oxford Medical Publications, 1998:320.

128. Bengis RG, Veary CM. Public health risks associated withthe utilisation of wildlife products in certain regions of Africa.Rev Sci Tech 1997; 16:586–593.

129. Young E, van den Heever LW. The African buffalo as asource of food and by-products. J S Afr Vet Assoc 1969;40:83–88.

130. Young E, Wagener LJJ, Bronkhorst PJL. The blue wilde-beest as a source of food and by-products: the productionpotential, parasites and pathology of free-living wildebeestof the Kruger National Park. J S Afr Vet Assoc 1969;40:315–318.

131. Young E, Wagener LJJ. The impala as a source of food andby-products. Data on production potential, parasites andpathology of free-living impalas of the Kruger National Park.J S Afr Vet Assoc 1968; 39:81–86.

132. Bengis RG. Animal health risks associated with the trans-portation and utilisation of wildlife products. Rev Sci Tech1997; 16:104–110.

133. Bengis RG.Wildlife diseases of animal and public health sig-nificance in the Kruger National Park. Proceedings of theSymposium on Wildlife Utilization in Southern Africa, 28June–6 July, 1992; Pretoria: National Parks Board.

134. Bengis RG. A review of bovine brucellosis in free-rangingAfrican wildlife.Proceedings of the ARC-Onderstepoort OIEInternational Congress with WHO-Cosponsorship onAnthrax,Brucellosis,CBPP,Clostridial and Mycobacterial Dis-eases, Berg-en-Dal, Kruger National Park, South Africa,9–15 August 1998.Onderstepoort:Onderstepoort VeterinaryInstitute, 178–183.

135. Gradwell DV, Schutte AP, van Niekerk CA, Roux DJ. Theisolation of Brucella abortus biotype I from African buffalo inthe Kruger National Park. J S Afr Vet Assoc 1977;48:41–43.

136. Chaparro F,Lawrence JV,Bengis R,Myburgh JG.A serologicalsurvey for brucellosis in buffalo (Syncerus caffer) in the KrugerNational Park. J S Afr Vet Assoc 1990; 61:110–111.

137. Young E,Whyte IJ.Trichinosis (Trichinella spiralis infestations)in wild animals of the Kruger National Park. J S Afr Vet Assoc1975; 46:233–234.

138. Young E.Echinococcosis (hydatodosis) in wild animals of theKruger National Park. J S Afr Vet Assoc 1975; 46:285–286.

139. Huchzermeyer FW. Public health risks of ostrich and croc-odile meat. In: Ahl AS, Sutmoller P, eds. Contamination ofanimal products: prevention and risks for public health. RevSci Tech Off Int Epiz 1997; 16:599–604.

140. Dauth J, Dreyer JM, Raubenheimer EJ, et al. Blood leadconcentrations in hippopotami (Hippopotamus amphibius) inthe Kruger National Park. J S Afr Vet Assoc 1988;59:153–154.

141. Fourie PB,Weyer K.Tuberculosis prevalence and risk of infec-tion in Southern Africa. S Afr J Sci 1986; 82:387.

142. Durrheim DN, Speare R, Govere J. Southern African schis-tosomiasis—epidemiology and control. In:Coetzer PWW,ed.The ecology of environmental hygiene and occupationalhealth. Pretoria: Easilearn CC, 1997:310–321.

143. Pitchford RJ. Temperature and schistosome distribution inSouth Africa. S Afr J Sci 1981; 77:252–261.

144. Appleton CC,Ngxongo SM,Braack LEO, le Sueur D.Schis-tosoma mansoni in migrants entering South Africa fromMozambique—a threat to public health in north-easternKwaZulu-Natal? S Afr Med J 1996; 86:350–353.

145. Pitchford RJ. Some brief notes on schistosomes occurringin animals. J S Afr Vet Med Ass 1963; 4:613–618.

146. Pitchford RJ, Visser PS. Excretion of Schistosoma mattheeieggs from man,baboons and cattle living in their normal envi-ronment. J Helminthol 1975; 49:137–142.

147. Pitchford RJ,Visser PS,du Toit JF, et al.Observations on theecology of Schistosoma mattheei Veglia & Le Roux, 1929, inportion of the Kruger National Park and surrounding areausing a new quantitative technique for egg output. J S AfrVet Assoc 1973; 44:405–420.

148. Murray C,Lopez A.Mortality by cause for the eight regionsof the world: global burden of disease study. Lancet 1997;349:1269–1276.

149. Van der Spuy JW.Trauma,alcohol and other substances.S AfrMed J 2000; 90:244–246.

150. Van der Spuy JW. South African road traffic statistics:1950–1994. Trauma Emergency Med 1996; 13:35–38.

151. Hargarten SW. Injury prevention: a crucial aspect of travelmedicine. J Travel Med 1994; 1:48–50.

152. Leggat PA,Durrheim DN,Apps PJ.Occupational risks posedby wild mammals in South African wildlife reserves. J OccupHealth Safety—Aust N Z 2000; 16:47–54.

153. Durrheim DN, Leggat PA. Risk to tourists posed by wildmammals in South Africa. J Travel Med 1999; 6:172–179.

154. Leggat PA,Durrheim DN,Braack LEO.Traveling in wildlifereserves in South Africa. J Travel Med 2001; 8:41–45.

155. Broadley DG. FitzSimons’ snakes of southern Africa. Johan-nesburg: Delta Books, 1983.

156. Fischhoff B, Bostrom A, Quadrel MJ. Risk perception andcommunication.Annu Rev Public Health 1993;14:183–203.

157. Leggat PA, Carne J, Kedyarune U. Travel insurance andhealth. J Travel Med 1999; 6:252–257.

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